Heat Stroke

Ann Disaster Med Vol 2 Suppl 2 2004

S97 Heat Stroke

From Department of Emergency Medicine, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, TaiwanAddress for reprints:Dr. Tzong-Luen Wang, Department of Emergency Medicine, Shin Kong Wu Ho-Su Memorial Hospital,No 95, Wen Chang Road, Taipei, TaiwanReceived: Feb 10 2004. Revised: Feb 20 2004. Accepted: Mar 10 2004.TEL: 886-2-28389425 FAX: 886-2-28353547 E-mail: [email protected]

Heat Stroke

Kuan-Che Lu, MD; Tzong-Luen Wang, MD, PhD

AbstractWhen psychological and physiologic adaptation mechanisms become dysfunction to environmentinduced a period of elevated heat stress, heat-related emergencies occur. Heat-related illness maybe trivial to life threatening. They represent a continuum of disorders such as heat edema, pricklyheat, heat cramps, heat tetany, heat syncope, and heat exhaustion to critical disease well known asheat stroke. It can be easily found in higher temperature situation such as the hot summer in Taiwanor those who have chronic medical diseases, older than 75 years, younger than 4 years, mentalillness, alcoholics, and vigorous exertion without proper training and acclimatization. Due to the highmortality is from 10 to 75 % in heat stroke, delay treatment after 2 hours onset of severe symptomsmay result in poor outcome. Early recognition and prevention become more important as earlyactually treatment. For the above reasons, the articles about heat stroke were reviewed to helpemergency physicians to be familiar with the heat related illnesses and cooling techniques and pro-vide optimal management for such victims.(Ann Disaster Med. 2004;2 Suppl 2:S97-S109)

Key words: Heat Stroke; Environmental Accident; Disaster Medicine

IntroductionThe increasing numbers of participants in manywilderness activities or adventure travelers inrecent years result in more environmentalaccidents. Studies of morbidity and mortality inNational Parks demonstrated an overall illnessand injury rate of 9.2/100,000 visits. Heat-re-lated illnesses are a spectrum of conditions rang-ing from mild illderness to life threatening heatstroke. It was also the most important and fre-quent cause of wilderness-related morbidity andmortality in the United States, responsible for 7%of wilderness-related deaths. Many militarycampaigns have been lost because of training

poor acclimatized troops with forced heavyphysical exercises. The U.S. Army reported atleast 125 deaths from heat stroke between 1941and 1944.1 Besides, 46 American football play-ers died of heat stroke between1961 and 1971.2 It is also the third leading cause of deathsamong American athletes. Heat-induced ill-nesses occur when body is unable to maintainappropriate homeostasis at the elevated ambi-ent temperature situation. This rise in body tem-perature may produce heat edema, heat rash,heat cramps, heat tetany, heat syncope, heatexhaustion, or heat stroke. Due to the highmontality of heat stroke, we review articles to


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help emergency physicians recognize and learnhow to manage the illness. Especially in mostsituations, heat illnesses may be preventablethrough many preventive methods and well pub-lic education with alarm for predictable heatwaves.

EpidemiologyHeat-induced illness is the most frequent causeof environment-related death in the U.S. Heat-related death rates average 1/1000000 forthose 5 to 44 years of age but increase to fivetimes in the population order than 85 years.From 1979 to 1999, 8015 heat-induced fatali-ties were reported to the C.D.C in the UnitedStates, and 3829 amoung them died of heatwaves (adverse weather condition). Analysis ofthe 3764 weather-related deaths revealed 142deaths and 1068 deaths fon those yunger than4 and olden than 75, respectively. Heat-induceddeath rate varies significantly according to theweather condition. In definition, heat waves are3 or more consecutive days of sustained tem-perature above 32.2 C. In the heat wave years1952 to 1955 and 1966, an average of 820annual heat stroke deaths were reported in theUnited States compared with 179 deaths pernonheat wave year. Despite advances in pre-vention and treatment, more than 700 deathswere induced by the heat during the 1995 heatwave in Chicago.3-4 Besides, 15 high school stu-dents died in heat stroke during football com-petition between 1995 and 2001. We foundthat athletes have higher risk to heat-related ill-nesses in vigorous exertion without propertraining, acclimatization, and fluid replacement.One California study about occupational heatinjuries indicated 1128 cases seeking medicaltreatment in a year. There were 7 deaths, 15 %

hospital admission rate, and 40 % workers offwork for several days after initial medicalmanagement. Populations at risk include: eld-erly ( age > 75 y/o ), younger ( age < 4 years )with congenital CNS disease or diarrhea illness, chronic illness or take some medications thatinterfere with heat loss or production such asantipsychotic drugs, anticholinergics,antiparkinsoniam drugs, B-blockers, calciumchannel blockers, diuretics, vasodilations,alcohol, amphetamine, cocaine, and ketamine.Other infreqnent situatious include congenitalabsence of sweat glands, scleroderma,hyperthyrodism, and pheochromocytoma. Inaddition, individuals with history of heat strokeare at greater risk for another episode. Anotherrisk factors are obesity, dehydration , and vig-orous exertion without proper training andacclimatization. The environmental risk factorsare high humidity, high temperature, and thosewithout air-condition breaks. Mortality of heatstroke ranges from 10 to 75 %. For those withsevere underlying disease or delayed treatmentfor more than 2 hours after the onset of severesymptoms, the rate would be hiqhen.

PathophysiologyBody temperature is regulated through a dy-namic balance between heat production (andabsorption) and heat loss.5 Heat is a byproductof cellular metabolism and the mechanical workof skeletal muscle. It is gained by direct con-tact with hot objects and radiation from the sun.The body heat is lost in four ways:(1) Conduction: represent direct heat transterinto cooler surrounding environment (eg. air,water, sweat, or clothes). When the surround-ing environment reaches the same temperatureas body skin surface, an insulator zone occurs


S99 Heat Stroke

and conduction stops. Since conduction of heatin water is thousand times than air, the insulatorzone will not be developed in the existence ofwater. So water or sweat is the primary deter-minant factor for heat loss.(2) Convection: is an adjunct to conduction,accounting for about 15% of total heat lossConvection fail to work when humidity and at-mosphere temperature above 35% and 32.2C,respectively.(3) Radiation: is the primary method when sur-rounding temperature lower than body tempera-ture and responsible for 60% body heat loss.(4) Evaporation of sweat into the surroundingair: is the primary way of heat loss when envi-ronmental temperature higher than body. Evenwithout sweating, respiratory and skin evapo-ration are responsible for 600 ml of water lossand 12 to 16 Kcal/h of heat loss pen day. Itaccounts for about 25% of heat loss in coolersituations and reaches nearly 100% at high tem-perature weather. The limitations are environ-mental humidity and whether adequate sweatamounts secretion is achieved. High humiditywill decrease the evaporation efficiency. Foreach 1% body weight dehydration, core tem-perature increases 0.1 to 0.3C. Furthermoredehydration, with fluid loss as high as 6-10%of body weight, appears to be the most com-mon risk factors for heat illness in exercisingindividuals in the heat.6 Dehydration also com-promises cardiovascular and thermoregulatoryadaptation by decreasing cutaneous blood flowand sweating rate. The Olympic athletes studyshowed that well acclimatized individuals getsweat secreting rate exceeding the ability ofwater absonption via qastrointestinal tract.Then, dehydration may occur. It is well knownthat sweating rate may be greater than 1 L/h.

Oral rehydration alone may be not enough.Convection and evaporation are more im-

portant than other methods of losing heat be-cause they are regulated primarily by the bodyitself. Wind velocity is also related to heatremoval. Heat loss is proportional to the squareroot of the wind velocity. But fan alone doesntlower the rate of heat stroke. According to theabove reason, lower socioeconomic statuspopulations without home air conditioning areat higher risk of heat-related illnesses.Furthermore, taking a heat break as short as 2hours a day will reduce the risk of heat strokeif no air-condition available.

The body have a diurnal temperaturechange, ranging from about 36C in the morn-ing to 37.5C in the afternoon.5 We tend to keepcore temperature between 36C and 38C.Theregulatory mechanisms fail to work when bodytemperature is above 40C or below 35C.Wecan stay at the temperature between 40C to42C for a short periods without severecomplications. Body temperature is regulatedby four primary methods including skinvasodilation, heat gain and production decreased(inhibit shivering), behavior heat control, andincreased sweat secretion. The anteriorhypothalamus, responsible for heat loss, re-ceives afferent information from cutaneous(surface) receptors and internal (core) tempera-tures and gives efferent signal to the skin bysympathetic nerves to stimulate skin vasodila-tation and sweating.7

Cutaneous vasodilatation increases con-vective heat loss.8 Sweating increase heat dis-sipation because of cooling the skin throughevaporation. When the hypothalamic set pointis normal and heat is produced or gained ab-normally or cannot be dissipated, the condition


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is known as hyperthermia. In contrast, whenthe hypothalamic set point elevate, it is wellknown as fever.5 Exposure to high tempera-tures and an elevation of body temperature willinduce a number of changes in the cutaneouscirculation. Skin blood flow is increased from abaseline of approximately 250 mL/minute to ap-proximately 6 to 8 L/minute through increasedcardiac output and concomitant vasoconstictionof the renal and splanchnic circulation. Cardiacoutput may increase nearly 3 L/min for each1C of temperature elevation. As the abovestatements, such victims may worsen the car-diovascular situation with underlying diseasesat this kind of condition. Arrhythmia, worsen-ing CHF, myocardial ischemia to infarction maybe developed. This change results in an increasein heat loss above the resting state of 80 to 90kcal/hour. Evaporation of sweat cools the skin,further enhancing heat transfer. Cutaneous di-lation and sweating increase as body tempera-ture rises until the heat dynamic balance regainedand body temperature elevation stopped. En-durance athletes and heat-enviroment workersmight reach and maintain body temperatures of40C (104F) without substantial morbidity.9

The human bodys response at hot climateto increase efficiency of heat loss is well knownas acclimatization, providing maximal heatlosing. Under the physiologic and biochemicaladjustments, individuals will adapt heat stressthat may result in others substantial morbidityor even death.10 It may take 7 to 10 days totarget the adaptation. The methods are moder-ate exercise in a hot and dry temperature situa-tion for 60 to 100 min per day or simple move-ment in the same situation for 1 to 4 hours perday. It can reach acclimatization within 2 weeks.When return to cold temperature, use the same

(1)Changing the amount and rate of sweating.(2)Increasing skin blood flow and cardiovas-cular function.(3)Changing the thermoregulatory set point:lower the thermal set point within thehypothalamus.

Acclimatization results in plasma volumeexpansion, increased renal blood flow, and in-creased ability to shunt blood away from non-critical circulatory areas (including the splanch-nic circulation), thus improving the renal resis-tance to exertional rhabdomyolysis. Acclimati-zation will also fasten activation of the renin-angiotension-aldosterone system, enhance thekidneys and sweat glands to retain sodium andprevent volume depletion. Despite this enhancedability to retain sodium, acclimated sweat glandscan actually secrete a greater volume of sweatby secreting sweat with significantly less tonicity,making volume depletion less likely and puttingthe heat-stressed individuals at less risk for vol-ume depletion or dilutional hyponatremia if fluidreplacement is maintained solely with free wa-ter or other non-electrolyte-containing solution.The acclimatization plans may be useful for spe-cific individuals such as soldier , athletes , oroccupational exposure workers. Those will pre-vent much heat induced illness and mortality.

Different mechanisms or pathologies be-tween exertional and non-exertional (classic)heat stroke willnt malce the final medical man-agement different. Emergency physicians mustsearch underlying drug history or illnesses tointerfere heat loss or production. Obesity guyshave less effective surface area and much adi-pose tissue (less water content amount), mak-ing heat loss ineffectively. Febrile diseases thatreset thermal point also worsen the heat release

time for adaptation. Primary routes are:


S101 Heat Stroke

the situation but play no role in truly environ-mental heat-related illness. Alcohol inhibitsADH. Confinement hyperpyrexia is a subtypeof non-exertional hyperpyrexia usually encoun-tered when children left inside the cars. It isfound that temperature reach up to 54C to60C within a locked car without ventilation inless than 10 minutes in hot weather. Illegalimmigrators within a closed box are also themajor problem in U.S.A.

Usually, heat causes damage to the bodyby three mechanisms: First, heat is directly dam-age to cells. Increasing cell temperature resultsin protein denaturation and interrupts criticalcellular processes, reading to apoptosis andcell death. Temperatures above 41.6C to42C are considered critical thermal maximumfor human beings and can be expected to pro-duce injury even in a few hours. Extremetemperatures, above 49C, result in nearly im-mediate cell death and tissue necrosis.

Second, heat induces release of inflam-matory cytokines including tumor necrosis fac-tor- , interleukin-1 () and interferon , andthe anti-inflammatory cytokines IL-6, IL-10,and TNF receptors p55 and p75. The elevatedtemperatures seem to result in vascular endot-helium injury, increased vascular permeability,activation of the coagulation cascades, and evendisseminated intravascular coagulation (DIC).

Finally, combination of direct cytotoxicityand severe systemic inflammatory responses inwhich encephalopathy predominates early in thecourse of the disease.10 If left unchecked, renalfailure, coagulopathy, hepatic dysfunction, andultimately multiple organ dysfunction systems

Clinical PresentationHeat edemaHeat edema occurs when cutaneous vasodila-tation and pooling of interstitial fluid in depen-dent extremities result in swelling of the handsand feet. It is a self-limited process for the firstfew days in hot situation and rarely lasts morethan a few weeks. Increased secretion ofantidiurentic hormorce and aldoslerone in re-sponse to the heat stress also contribute to someedema formation. It is easily found in non-ac-climatized and elderly human or during travel-ing in airplanes or cars from a colder climate toa hotter environment. Pitting edema over anklesmay be seen but pre-tibia area is never involved.Treatments includes elevation and applicationof compressive stockings or support hose ofthe extremities. Diuretics should avoided be-cause of potential volume depletion, and elec-trolyte imbalance.

Prickly HeatIt is a maculopapular, pruritic, and erythema-tous rash over the clothes covered areas, whichis well known as heat rash or miliaria rubra.The etiology is that sweat gland duct pores areblocked. In acute phase, it can be easily treatedby antihistamines. Other preventive maneuversare wearing clear, light, and bigger clothes thanusual to facilitate heat loss. Besides, baby pow-der is of no value in the situation and may inter-fere sweating and heat loss. Chlorhexidine lo-tion or light cream can be the alterative treat-ment choice. In severely cases, damage involvesdeep into the dermis causing white and non-pruritic papules, which may progress intochronic dermatitis and associate with Staphy-lococcus aureus infection. Antibiotics like ox-acillin or erythmycin may be useful in this kind

from our skin. Antipyretics may be helpful in

will result.


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situation. In addition, using 1% salicylic acidthree times a day can cause desquamation ofthe involved skin.

Heat CrampThe illnesses are characterized by painful,involuntary, and self-limited muscle spasms, es-pecially involved the large muscle groups suchas he calves, thighs, and shoulders.Its oftenoccurred several hours after vigorous exercisein a hot environment and during a rest period ofshowering. Common for non-acclimatized in-dividuals just beginning to receive training. Hy-pokalemia combined with hyperventilation is alsoconsidered a predisposing factor. Dilutionalhyponatremia will be deueloppd because indi-viduals replace sweat loss with free water with-out salt contents.11-13 Core body temperaturemight be normal or elevated. Managements in-clude resting in a cool environment and saltreplacement. Oral electrolyte solution with com-mercially available balanced sports drinks or650 mg sodium chloride tablet in 500 ml water(about 0.1 to 0.2% saline solution) are thechoices. Rarely, intravenous normal saline isrequired. In addition, the pain will not be re-lieved by opiates alone, and occurred in the ab-sence of other symptoms includingrhabdomyolysis. Neventhless, they can be ac-companied by symptoms and signs of heatexhaustion.

Heat TetanyIt is the condition that hyperventilation syndromeoccurred under the heat stress, like the typicalhyperventilation presenting with paresthesia ofextremities and circumoral area, respiratoryalkalosis, and carpopedal spasm. It results inlittle pain and cramps than heat cramps.

Otherwise, more paresthesis over specific ar-eas are noted than heat cramps. Managementsinclude lowering the respiratory rate and rest-ing in a cool environment.

Heat SyncopeHeat syncope results from volume depletion,peripheral vasodilatation, pooling of bloods anddecreased vasomotor tone while exercising ina hot environment, with subsequent transient lossof consciousness. It affects most commonly inpoorly acclimatized and elderly individuals. Re-covery after supining and usually normal bodytemperature separate heat syncope from heatstroke. Postural hypotension might or might notbe noted on presentation to the emergencydepartment. The key points should be thoroughevaluation for injuries induced by a fall, andexclud all cardiac, neurologic, or other poten-tially serious causes of syncope. Treatmentsconsist of rest and oral or intravenous fluid sup-ply in a cool environment. Education of victimsto prevent damage from fall is important as weu.

Heat ExhaustionHeat exhaustion is the most common heat-re-lated illness14 and characterized by significantvolume depletion.15 Classically, heat exhaustionis classified as water depletion and saltdepletion. Water depletion heat exhaustion oc-curs in individuals working in a hot environmentwithout adequate water replacement.Nevertheless, salt depletion heat exhaustiontakes longer time to develop and occurs duringexercise in a hot environment because of heavysweating and hypotonic solutions replacement.But most victims presenting to ED always com-bine with both water and salt loss. Those whohave heat exhaustion will present with nonspe-


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cific systemic symptoms and signs such asfatigue, headache, nausea, vomiting, weakness,malaise, dizziness, myalgia, irritability, diaphore-sis and muscle cramps. Patients can also expe-rience orthostatic hypotension or heat syncope.Physical examination usually shows core tem-peratures of less than 40C and normal mentalstatus. As physical response for heat stress, vic-tims may present to ED with tachycardia, ortho-static hypotension, and clinical evidence ofdehydration. Patients who have heat exhaus-tion will usually have profuse sweating almost.

Mild heat exhaustion and heat stroke areat opposite ends of the heat illness diseasespectrum. We sometimes have difficulties to dif-ferentiate from them. Anhidrosis, CNSdysfunction, and body core temperature above40C are clues. Exertional heat stroke may ini-tially present to ED without anhidrosis. Besides,heat stroke may occur at any core temperatureespecially when the patients with heat strokehad been treated before arriving to ED. If anydoubt in differentiating from the two kinds ofsituations, the patients should be treated for heatstroke as soon as fast. In fact, heat stroke mayhappen if heat exhaustion left untreated. Alwayskeep in mind that heat exhaustion is a diagnosisof exclusion. The only objective and usefulmethod is the level of hepatic enzymes. It isfound elevated in heat stroke and may contrib-ute to the delayed complications of heat stroke.

Laboratory abnormalities, includinghemoconcentration, hyponatremia orhypernatremia can also be measured. In heatexhaustion, altered mental status or seizureswithout combination with severe hyperpyrexia,hypoglycemia,or trauma may alert the physi-cians that hyponatremia maybe the primaryetiology, especially if symptoms progress after

exercises stop. Therapies consist of increasedheat loss by fan evaporation, rest in a coolsituation, salt with fluid repletion. Oral sportsdrinks is acceptable in those without unstablevital signs or have severe vomiting. On the otherhand, electrolytes measurement and intravenousnormal saline may achieve the better efficiencyif the victims are hemodynamically unstable orsevere GI upset. Furthermore, avoid exercisefor 2 to 3 additional days needs to be informed.Hospital admission is rarely acquired except vic-tims of CHF or severe electrolyte imbalance.

Heat StrokeClassic heat stroke. Classis heat stroke istypically seen in debilitated patients after sev-eral days of high environmental temperaturesand humidity exposure. This condition is seenmost commonly during heat waves. Individualsespecially at highen risks include those who arechronic ill, the elderly, alcoholic abuse, thosewithout air conditioning. Others taking specificdrugs as previously mentioned are also at par-ticular risks.16 Chronic and debilitating diseasessuch as cardiac conditions, dementia, andchronic obstructive pulmonary disease havealso been found at risk.17 In addition, infantsand ill, febrile children are at highen risk.18 Oneanimal study streptozotocin-induced diabeticrats to demo that chronic illness such as DM ismore easily induced to elevated striatalglutamate (represent more serious heat-shocksyndrome) by high temperature exposure. Sothat, insulin treatment seems helpful in the pre-vention of heatstroke in STZ-diabetic rats.19

Two major diagnostic findings are core tem-perature more than 40C and CNS dysfunction.10 Typically, victims may be anhidrosis, but ab-sence of sweat is not the absolute diagnostic


Heat Stroke S104

criterion. Follow the rule might lead to a delayin the diagnosis and treatment of heat strokewith serious complication.20 CNS dysfunctionis usually manifested by delirium, seizures, orcoma. Other clinical findings such ashallucinations, ataxia, or bizarre behavior canalso be noted. Patients can also present withsystemic symptoms like nausea and vomitingsimilar to heat exhaustion but with altered men-tal status. Besides, most will present with ta-chycardia and hypotension when arrival to ED.17,21

Hyperventilation, with concomitant meta-bolic acidosis, is also common.5,22 Unfortunately,more than 50% may be combined with infec-tion at presentation. This might be explained bythat increased leukocyte count with decreasedcirculating neutrophil phagocytic capacity andincreased expression of lymphocyte adhesionmolecules increase susceptibility to infectionsin exertional heat stroke.23 Laboratory findingsmight include hemoconcentration, acute renalfailure (ARF), abnormal liver function tests,hypernatremia or hyponatremia, and hypokale-mia according to the degree of dehydration.17,20

Exertional heat stroke. Exertional heat strokeis found more commonly in poorly acclimatizedyoung persons involved in vigrous physical ex-ercise under a hot environment. It can be typi-cally found in healthy military soldiers, miners,and athletes20 particularly if they lack watersupply. In retrospective analyses, most of thecases can be preventable.24 It presents similarsymptoms as classic heat stroke, except pro-fuse sweating,14,25 account of that 50% casesare still sweating at presentation. Vomiting anddiarrhea are relative more common, occurringin up to two thirds of patients.26 25 % of pa-tients will develop ARF.14 Rhabdomyolysis,

exertional heat stroke. Laboratory abnormali-ties are similar to classic heat stroke. Hypokale-mia is developed in early stages, with hyper-kalemia manifesting later. Sodium levels can benormal or slightly elevated depending on the hy-dration status of the patients. Elevated creati-nine phosphokinase (CPK) secondary torhabdomyolysis may be seen. Those who havepeak CPK levels above 10,000 IU/L are atsignificant risk to develop ARF.27 However, lowlevels of CPK on initial measurement do notrule out the development of ARF.28 Besides,marked lactic acidosis, hypocalcemia, and hy-poglycemia can also be seen. Differ from clas-sic heat stroke from another form have no clinicalvalue due to result in the same treatment. Thedetermine factor affect mortality is the underly-ing diseases other than the height of coretemperature.10,29-30 Heat stroke is the diagnosisof exclusion. It include such as drug withdrawalsyndrome, ethanol withdrawal, neurolepticmalignant syndrome, systemic infection, CNSinfection, DKA, thyroid storm, Intracerebralhemorrhage, status epilepticus, serotoninsyndrome, drug toxicity(anticholinergics ,amphetamines, etc).So, clinical laboratory sur-vey must be ordered to detect end organ dam-age and to rule out other etiology that may mimicheat stroke.31

TreatmentRemove the victim immediately from hot con-dition to a cool shaded area. Take off all cloth-ing and evaluate the adequacy of airway,breathing, and circulation following as ACLSguideline suggestion. Rapid cooling the coretemperature to below 40C is the only goal andshould not be delayed if any method is available.Cold water or ice water immersion should beARF, and DIC are more common in victims of


S105 Heat Stroke

instituted if readily available and lower tempera-ture more rapidly although disadvantages suchas shivering, monitor lead disconnection, equip-ment less available, primary in young and heathvictims without comorbid diseases. In a studyof 252 exertional heat stroke cases, ice waterimmersion lowered core temperature to below39C within 10 to 40 minutes without fatalitiesin this group.32 In another study, ice water im-mersion cooled twice as fast as evaporativecooling.33 Alternatively, evaporative cooling byspraying water over the patients skin and fan-ning the patient maybe useful in pre-hospitalsetting and receiving facility.34 Ice packs are alsofrequently used in ED and placed over the neck,axillae, and groin. However, several studies havenot shown a significant reduction of cooling timewith their use.35-36 Finally, a core temperatureshould be checked with serial monitoring by anelectronic rectal thermistor probe or tempera-ture probe-equipped urinary drainage catheterduring the cooling process to ensure adequatecooling and to prevent iatrogenic hypothermiaand rebound of hyperthermia requiring furthertreatment. If patient is intubated, esophagealthermometer is another choice. If equipment islimited, use tympanic thermometer as frequentas possible every 5 to 10 minutes. Seizures andexcessive shivering can be managed by usingthe benzodiazepine

Intravenous LR or NS at a rate of 250ml/hr is advised for most patients. Fluid challengemust be adjusted by underlying conditions, urineoutput, serial BP monitor, and PCWP or CVP.An animal study result demonstrates that theneuroprotective effect of hypervolaemichaemodilution by NS supply decrease cerebralischaemia and hypoxia injury in heat stroke rats.37

Another study using 3% hypertonic saline in

heat stroke rats shows a better heat stroke syn-drome preventive effect than NS.38 Random-ized and larger clinical trials are pivotal beforewidely use. Dopamine causes peripheral vaso-constriction at higher doses and impaired cuta-neous perfusion and heat loss. Glucose levelmust be checked at bedside since hypoglyce-mia can be noted in exertional heat stroke.Hematocrit, electrolytes, BUN, creatinine, liverfunction tests, CPK, coagulation studies, andurinalysis should be measured. Electrolytes andmetabolic abnormalities should be correctedappropriately. Other complications such asrhabdomyolysis, ARF, DIC, or liver damageneed to be evaluated and treated. The majorityof patients having exertional heat stroke will re-cover without sequelae.25 Long-term effects forheat stroke survivors are rare with adequatetreatment. In a casecontrol study of 21 youngpatients suffering exertional heat stroke followedup for 6 months and tested for heat toleranceand psychological sequelae, none was foundto have any abnormal findings.39 Moderate tosevere residual neurologic defects in classic heatstroke survivors have been reported in up to33% of cases.21 Neurologic deficits areparaplegia, paresis, dysarthria, memory loss,concentration difficulty, and ataxia.25 With ap-propriate rehabilitation, significant motor andcognitive function can be recovered over time.40

A randomized, controlled, prospective ratmodel demonstrated that direct retrograde hy-pothermic perfusion via the external jugular veinprotected the brain after heatstroke. This tech-nique cooled the brain without significantly in-terfering body temperature.41 Another studyshowed that although pretreatment with alpha-tocopherol and mannitol did not prevent the heatstroke syndrome entirely, an attenuation of the


Heat Stroke S106

syndrome is observed.42 But it is still contro-versial and may induce osmotic diuresis andcompromise dehydration.

DispositionAll heat-related illness may be discharged foroutpatient follow-up except(1) Heat exhaustion combined with

extremityage,significant electrolyteorfluid disturbance, severe underlyingdiseases, or end organ damage.

(2) Heat stroke.

PreventionPrevention remains the most important methodfor heat-induced illnesses. Always keephydration, wear adequate clothing, aware of riskfactors and weather prediction especially theheat wave from TV or newspaper can preventmost heat injuries. Elderly patients at risk forclassic heat stroke should be evaluatedfrequently. Avoid strenuous physical activitiesduring extreme hot weather with frequent heatbreak and adequate fluid and salt supply isessential. Overhydration should be avoidedsince severe hyponatremia have been reportedin marathon runners, especially in women andslow runners, due to excessive fluidconsumption.43 White or light-colored clothingreflects radiant energy is also helpful.

SummaryThe majority of heat-related illnesses can beprevented by adequate fluid and electrolytessupply and awareness of potential risk factors.Familiarity of emergency physicians and primaryphysicians is fundamental for early diagnosis andtreatment. Public education is essential as well.

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